PROGNOSTIC SIGNIFICANCE OF SST2 IN HEART FAILURE WITH REDUCED EJECTION FRACTION, A BIOMARKER OF CARDIOVASCULAR MORTALITY AND REHOSPITALIZATION.

Introduction: Heart failure (HF) poses a substantial burden on healthcare systems and society, necessitating effective diagnostic tools for enhanced patient management. The soluble suppression of tumorigenesis 2 protein (Soluble Suppression of Tumorigenesis 2 (sST2)) has emerged as a promising biomarker linked to cardiac remodeling and fibrosis. This study investigates Soluble Suppression of Tumorigenesis 2 (sST2)'s potential as a diagnostic and prognostic marker for chronic heart failure (CHF) and explores its clinical utility in predicting outcomes.

Aims And Objectives: To evaluate the utility of Soluble Suppression of Tumorigenesis 2 (sST2) as a predictive and diagnostic marker in patients with heart failure with reduced ejection fraction (HFrEF). The study aims to explore the connection between Soluble Suppression of Tumorigenesis 2 (sST2) levels and cardiovascular (CV) mortality in patients suffering from chronic heart failure (CHF), providing insights into how Soluble Suppression of Tumorigenesis 2 (sST2) levels correlate with patient outcomes. Additionally, it seeks to assess the ability of Soluble Suppression of Tumorigenesis 2 (sST2) to predict critical clinical events such as hospital readmissions and adverse 02composite outcomes, offering a deeper understanding of its potential role in disease management. Furthermore, the research compares the prognostic accuracy of Soluble Suppression of Tumorigenesis 2 (sST2) with NT-proBNP, a well-established biomarker, to determine which marker is more reliable and informative for predicting the progression and severity of CHF.

Methods: This prospective cohort study included 111 CHF patients enrolled from May 2020 to January 2022. Participants were classified into two groups based on their Soluble Suppression of Tumorigenesis 2 (sST2) concentrations (<35 ng/mL and >35 ng/mL) and monitored over a year. Comprehensive demographic, clinical, and echocardiographic data were collected, alongside blood samples for Soluble Suppression of Tumorigenesis 2 (sST2) and NT-proBNP analysis. Kaplan-Meier survival analysis, Cox regression modeling, and chi-square tests were employed, with statistical significance defined as P < 0.05.

Results: Patients with Soluble Suppression of Tumorigenesis 2 (sST2) levels above 35 ng/mL experienced a markedly higher one-year cardiovascular (CV) mortality rate of 27.3%, compared to just 2.2% in those with lower levels. Similarly, elevated Soluble Suppression of Tumorigenesis 2 (sST2) levels were strongly associated with an increased risk of hospital readmissions, as 27.3% of high-Soluble Suppression of Tumorigenesis 2 (sST2) patients required multiple hospitalizations within a year, compared to only 2.3% in the low-Soluble Suppression of Tumorigenesis 2 (sST2) group. In contrast to NT-proBNP, Soluble Suppression of Tumorigenesis 2 (sST2) levels were not affected by factors like age or kidney function, making it a more reliable and consistent marker of cardiac remodeling. Additionally, patients who did not show a reduction in Soluble Suppression of Tumorigenesis 2 (sST2) levels were significantly more likely to face adverse composite outcomes, with 45.5% affected, compared to 12.4% among those whose levels decreased.

Conclusion: Soluble Suppression of Tumorigenesis 2 (sST2) has emerged as a valuable prognostic biomarker for CHF, offering advantages over NT-proBNP due to its independence from confounding factors such as renal function and atrial rhythm. Elevated Soluble Suppression of Tumorigenesis 2 (sST2) levels are strongly correlated with increased mortality, hospitalizations, and adverse outcomes. While baseline Soluble Suppression of Tumorigenesis 2 (sST2) levels provide meaningful insights into disease severity, short-term changes are less indicative of prognosis. Integrating Soluble Suppression of Tumorigenesis 2 (sST2) into routine clinical practice could improve CHF management by enabling early identification of high-risk patients and guiding personalized treatment strategies.